Balding is caused by DHT

@Clavicular @Gengar when botb
 
Does DTH affect acne in adult males? And can i reduce acne on my back and shoulders by taking fin
 
Does DTH affect acne in adult males? And can i reduce acne on my back and shoulders by taking fin
i am pretty sure dht type 1 is responsible for acne, so you need to take dutasteride

And yes dutasteride is proven to reduce acne but would this also reduce acne from the back (probably, i can later look at the scientific literature about it)

Btw acne on the back is not normal.. do you use steriods? Or consume any dairy?
 
Last edited:
  • +1
Reactions: Eblan
So if I am not roidmaxing should I just use fin and how much, note: I am 20 years old my dad doesn't have a hairline just hairs grown on the sides and a few on top and on my mom's side her brother is bald, my hair is also 1a type and really fine and thin though my hairline doesn't look the worst its not ideal so I think I should start on fin and oral minox before any problems start happening. Also where would I be able to buy fin online? instead of going to a doctor or somewhere unless i can get it without a subscription. Thanks sm and this thread is goated btw.
 
So if I am not roidmaxing should I just use fin and how much, note: I am 20 years old my dad doesn't have a hairline just hairs grown on the sides and a few on top and on my mom's side her brother is bald, my hair is also 1a type and really fine and thin though my hairline doesn't look the worst its not ideal so I think I should start on fin and oral minox before any problems start happening. Also where would I be able to buy fin online? instead of going to a doctor or somewhere unless i can get it without a subscription. Thanks sm and this thread is goated btw.
1 mg fin + topical minoxidil

There are sites that sell finasteride online like this one
 
  • +1
Reactions: ZyBurg
So if I am not roidmaxing should I just use fin and how much, note: I am 20 years old my dad doesn't have a hairline just hairs grown on the sides and a few on top and on my mom's side her brother is bald, my hair is also 1a type and really fine and thin though my hairline doesn't look the worst its not ideal so I think I should start on fin and oral minox before any problems start happening. Also where would I be able to buy fin online? instead of going to a doctor or somewhere unless i can get it without a subscription. Thanks sm and this thread is goated btw.
1 mg fin + topical minoxidil

There are sites that sell finasteride online like this one
You can easily get some sites that sell fin in you country

There are many online dr sites that sell you the medicine and precription
 
  • +1
Reactions: ZyBurg
You can easily get some sites that sell fin in you country

There are many online dr sites that sell you the medicine and precription
Thx for this source and why not oral minox, does topical just work better? what if I am also trying to grow eyelashes and eyebrows?
 
i am pretty sure dht type 1 is responsible for acne, so you need to take dutasteride

And yes dutasteride is proven to reduce acne but would this also reduce acne from the back (probably, i can later look at the scientific literature about it)

Btw acne on the back is not normal.. do you use steriods? Or consume any dairy?
Yes, I consume dairy daily and do not use steroids
 
DHT is obviously involved but it's clear from the crazy results some people get from deep microneedling, botox scalp injections and hard scalp massages that in many cases Norwooding is caused by fibrosis, calcification restriction of blood supply and head shape mechanical tension etc. The stresses to the scalp and lower oxygen environment is a signal for excessive DHT to park itself there and do it's final kill shot on the hair follicles. Females having low DHT and high estrogen avoid that fate usually. I think estrogen is the only way a Norwood 6 has ever got their hair back - by doing a transvestite sex change.
Do you know a mtf trans who got thier hair back by only hrt and not getting a hair transplant?
 
evolution absolutely cares about beauty, because in europe, women were in very equal standing to men, unlike in other parts of the world (at least in bronze age north europe)
It could be true, I have seen women jn thier prime with balding men/ completely balded nw7
 
What do you think about taking glycine supplement? Will it increase DHT while on dut?
Nahh i did some research

And no, i barely found any studies about it
I only found one that show the opposite fact here in this article

dont worry about it
 
Nahh i did some research

And no, i barely found any studies about it
I only found one that show the opposite fact here in this article

dont worry about it
Glycine is a nice softmax as it is the most abundant amino acid in collagen. Also, what about creatine? I heard it is a nuke for follicles, even people on fin reported hair loss
 
BALDING (ANDROGENETIC ALOPECIA) IS CAUSED BY DHT
the strongest evidence I can think of right now.. If it's not enough to convince someone of the causal role of androgens in baldness then that person is brain dead or willfully ignorant.

Common male pattern baldness is a highly heritable trait which requires the presence of androgens. The official name is androgenetic alopecia (AGA), which is a compound word for androgens+genetics and hair loss, meaning that both of these are required for it to occur. It refers to the specific type of hair loss in the horseshoe (Norwood) pattern that is caused by androgens, specifically DHT, and a genetic predisposition. The onset and severity of baldness can be predicted with high accuracy based on your genes.[16] These are the facts, it is so accepted in the medical community that these are the two causes of AGA that the very name of the disease is derived from them. Twin and genomic studies estimate the heritability of AGA to be around 80% for early and late-onset, with genetic influence of clear-cut vertex balding reaching as high as 89% and frontal recession reaching 96%, in young individuals[7][8]. In a study of 553 men, 92% of older men with baldness had a polymoprhism in the Stu1 restriction site of the androgen receptor, while only 76.6% of men without hair loss had this polymorphism, while 98% of men with premature baldness had it. There was only one balding young man out of 52 who did not have it.[17] He may have had other polymorphisms of the AR, and/or a lot of risk alleles in genes that are causal downstream of the AR. The significance of this finding has been confirmed several times. This is just one of many SNPs regulating the AR gene, yet it has a significant predictive effect on baldness, highlighting the importance of androgens in the etiology of AGA, and the requirement for a genetic predisposition.

View attachment 3391498
This shows the difference that just a single SNP on a single gene (AR) makes on the probability of going bald.[17] You are more than twice as likely to develop any balding or severe balding if you have the risk allele for this SNP. There are many other genes which interact with the AR and pathways regulated by androgens that have a significant effect. The combined effect of all of these genes makes baldness highly heritable. There is some environmental component, which has a minor effect on the severity or age of onset, but it would not be possible to induce common baldness in someone who is not genetically predisposed to it. Native American men without admixture, for example, do not go bald regardless of their lifestyle, nor do they have significant body hair[18].

Men with Klinefelter syndrome, i.e. born with an extra X chromosome causing androgen deficiency, do not go bald[22]. Men with androgen insensitivity syndrome, caused by a mutation in the AR gene making them insensitive to androgens, also do not go bald, with two exceptions of FPHL in the literature[21][23]. Pseudohermaphrodites who have a genetic mutation blocking the production of 5-alpha reductase type II are immune to baldness[19][20][32]. This is the enzyme that converts testosterone into the more potent metabolite dihydrotestosterone (DHT). It was the observation of no baldness in these pseudohermaphrodites which prompted the development of Propecia (finasteride) to treat baldness. The drug binds to and blocks the action of the enzyme 5ar-II, which is produced by the gene SRD5A2. Genetic studies have also identified this gene as causal in the development of AGA. When controlling for age, ethnicity, etc., men with variants of this gene that increase production of the enzyme have a significantly higher risk of going bald[9].

The effects of DHT on the hair follicle are mediated by binding to its receptors, the androgen receptor, this allows the androgen receptor to translocate into the nucleus of the cell where it can bind DNA and regulate gene transcription. The AR, the gene that produces the androgen receptor, shows an even stronger genetic association with baldness than SRD5A2. Polymorphisms of this gene show the strongest association with baldness of any gene. There is a disease called Kennedy disease, which is caused by extended CAG repeats in the AR gene. Repeats reduce the sensitivity of the AR gene to activation. Men with this disease are protected against baldness. The more repeats they have the less likely they are to go bald.[1][9]The application of androgens to hair follicles ex vivo retards their growth.[25][26][27] Even when hair follicle cells are removed and exposed to androgens in vitro it reduces their proliferation, the effect of which is reversed by coculture with an androgen receptor antagonist. Only dermal papilla cells from human and macaque hair follicles which are subject to AGA show reduced hair cell proliferation in response to androgens. It does not affect hair follicles on the back of the head.[10][24] Removing the AR or DHT prevents the gene transcription changes that take place in frontal hair follicles.[2] Treatment with androgens inhibits differentiation of hair follicle stem cells by inhibiting the Wnt pathway.[28]

Bald scalp has higher levels of DHT, AR and SRD5A2 than healthy scalp.[3][4][15] In all primates, men do not go bald before reaching sexual maturity. Macaques go bald within months of reaching puberty when androgens are produced. Their baldness represents a hypoplastic change in the type of hair follicle from terminal to vellus similar ,but in the opposite direction, to the hypoplastic change androgens cause in body hair after puberty. [6][29]. This is due to the known differential growth responses that androgens have on genetically identical hair follicles, which varies due to site-specific epigenetic programming.[30] Men who were castrated as juveniles do not go bald, but when injected with testosterone they do. Cessation of testosterone treatment in eunuchs, or castration of balding men, prevents further baldness, but does not reverse baldness[5]. Finasteride prevents baldness in monkeys.[14] Finasteride and dutasteride are highly selective drugs that inhibit only the enzyme responsible for producing DHT. Finasteride, which reduces scalp DHT by 64%[31], prevents baldness in 86% of men after a 10 year follow up[11], and 99% of Japanese men[12]. The more potent dutasteride halted baldness in 94% of men after 5 year follow up[12]. Genetic knockout of SRD5A2 or AR would prevent it in all men who don’t have a rare mutation in one of the genes downstream of the AR.

1 https://academic.oup.com/bjd/article-abstract/157/2/290/66408662 https://www.nature.com/articles/s41597-022-01846-w3 https://academic.oup.com/jcem/article-abstract/39/6/1012/26855274 https://www.nature.com/articles/s41598-023-48942-45 https://onlinelibrary.wiley.com/doi/10.1002/aja.10007103066 https://link.springer.com/chapter/10.1007/978-3-642-74612-3_187 https://link.springer.com/chapter/10.1007/978-3-642-74612-3_188 https://pubmed.ncbi.nlm.nih.gov/16127116/9 https://www.nature.com/articles/s41467-017-01490-810 https://pubmed.ncbi.nlm.nih.gov/8977424/11 https://pubmed.ncbi.nlm.nih.gov/21910805/12 https://pubmed.ncbi.nlm.nih.gov/38321615/13 https://www.oatext.com/Long-term-(1...3-Japanese-men-with-androgenetic-alopecia.php14 https://pubmed.ncbi.nlm.nih.gov/1309834/15 https://academic.oup.com/jcem/article-abstract/38/5/811/26854011 6 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441445/17 https://link.springer.com/article/10.1007/s00439-006-0317-81 8 https://www.belgraviacentre.com/blog/native-americans-and-hair-loss19 https://pubmed.ncbi.nlm.nih.gov/25321150/ 20 https://www.science.org/doi/10.1126/science.186.4170.121321 https://www.ncbi.nlm.nih.gov/books/NBK430924/ 22 https://karger.com/sad/article/7/2/135/291539/Androgenetic-Alopecia-in-a-Patient-with 23 https://pubmed.ncbi.nlm.nih.gov/8092978/24 https://www.spandidos-publications.com/10.3892/mmr.2015.3478?text=fulltext 25 https://pubmed.ncbi.nlm.nih.gov/2078048/26https://www.eeose.com/UserFiles/Image/files/pdfler/caffeineno_b.pdf 27 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC698966028 https://pubmed.ncbi.nlm.nih.gov/22283397/29 https://pubmed.ncbi.nlm.nih.gov/7035577/ 30 https://pubmed.ncbi.nlm.nih.gov/29046359/31https://www.sciencedirect.com/science/article/pii/S0022202X1552935732https://pubmed.ncbi.nlm.nih.gov/4432067/ (bewerkt)

5-alpha reductase (5AR) inhibitors have barely or no side effects
5ar inhibitors have no side effects
I sended many good studies including meta analyses (The highest level of scientific proof) supporting this claim in this excellent thread

The FDA even did a investigation and found out that 5AR inhibitors have no sexual or depressive side effects

Don’t be scared of the DHT lovers in this forum and their pseudoscientific theories (which lack solid scientific evidence)
Their theories simply don’t happen in reality—it’s just yapping. They simply don’t happen.


WHAT DR NICKGA!! DHT IS NEEDED FOR BONEMASS AND AND..... (yapping)
It already got debunked in this thread (which they stole some of my arguments hehehehehehe) and this debate i had with a disgusting dht lover


NO NOOO NOOOOO BALDING IS CAUSED BY PROLACTIN AND UHH FAPPING!!
We males experience androgenetic alopecia
Balding in males is 99% caused by DHT, ANDROGENS
BALDING IS CAUSED BY HIGH LEVEL OF DHT IN THE SCALP COMBINED WITH HIGH LEVEL OF ANDROGEN RECEPTOR IN THE SCALP

the scalp tension bloodflow theory, the estrogen theory (low estrogen = balding) , the faping theoryy (......) and more
It’s all utter nonsense by the dht lovers
View attachment 3391607
View attachment 3391610View attachment 3391614View attachment 3391620View attachment 3391622View attachment 3391608
THESE PEOPLE ARE IDIOTS , VERY VERY DUMB IN THE PICTURES, IMAGINES ABOVE
including @ConfusedBolivian and @Jonas2k7 who also blamed serum prolactin causing androgenetic alopecia??????

this picturess , imagines are 0.00001 of the Psuedoscience and stupidity in .org


@piec @halloweed @Hexmask @DR. NICKGA
@piec @halloweed @Hexmask @DR. NICKGA
do retards really need this much proof to show that dht makes u norwood
 
Glycine is a nice softmax as it is the most abundant amino acid in collagen. Also, what about creatine? I heard it is a nuke for follicles, even people on fin reported hair loss
Barely research on that too

Only one very small bad study (rugby players) that creatine increased dht levels

Oh wel, if you say that even people on fin reported hairloss, you should not take the risk!
 
Barely research on that too

Only one very small bad study (rugby players) that creatine increased dht levels

Oh wel, if you say that even people on fin reported hairloss, you should not take the risk!
That's for sure, not worth for a tiny strength gain and bloated muscles
 
Do you know a mtf trans who got thier hair back by only hrt and not getting a hair transplant?

There were a few that did that were NW6 with no transplants. The NW3s mostly went back to normal hair also I think after some time. Forget the link where the pictures were posted.
 
  • +1
Reactions: averagenormie and Phillybeard1996
BALDING (ANDROGENETIC ALOPECIA) IS CAUSED BY DHT
the strongest evidence I can think of right now.. If it's not enough to convince someone of the causal role of androgens in baldness then that person is brain dead or willfully ignorant.

Common male pattern baldness is a highly heritable trait which requires the presence of androgens. The official name is androgenetic alopecia (AGA), which is a compound word for androgens+genetics and hair loss, meaning that both of these are required for it to occur. It refers to the specific type of hair loss in the horseshoe (Norwood) pattern that is caused by androgens, specifically DHT, and a genetic predisposition. The onset and severity of baldness can be predicted with high accuracy based on your genes.[16] These are the facts, it is so accepted in the medical community that these are the two causes of AGA that the very name of the disease is derived from them. Twin and genomic studies estimate the heritability of AGA to be around 80% for early and late-onset, with genetic influence of clear-cut vertex balding reaching as high as 89% and frontal recession reaching 96%, in young individuals[7][8]. In a study of 553 men, 92% of older men with baldness had a polymoprhism in the Stu1 restriction site of the androgen receptor, while only 76.6% of men without hair loss had this polymorphism, while 98% of men with premature baldness had it. There was only one balding young man out of 52 who did not have it.[17] He may have had other polymorphisms of the AR, and/or a lot of risk alleles in genes that are causal downstream of the AR. The significance of this finding has been confirmed several times. This is just one of many SNPs regulating the AR gene, yet it has a significant predictive effect on baldness, highlighting the importance of androgens in the etiology of AGA, and the requirement for a genetic predisposition.

View attachment 3391498
This shows the difference that just a single SNP on a single gene (AR) makes on the probability of going bald.[17] You are more than twice as likely to develop any balding or severe balding if you have the risk allele for this SNP. There are many other genes which interact with the AR and pathways regulated by androgens that have a significant effect. The combined effect of all of these genes makes baldness highly heritable. There is some environmental component, which has a minor effect on the severity or age of onset, but it would not be possible to induce common baldness in someone who is not genetically predisposed to it. Native American men without admixture, for example, do not go bald regardless of their lifestyle, nor do they have significant body hair[18].

Men with Klinefelter syndrome, i.e. born with an extra X chromosome causing androgen deficiency, do not go bald[22]. Men with androgen insensitivity syndrome, caused by a mutation in the AR gene making them insensitive to androgens, also do not go bald, with two exceptions of FPHL in the literature[21][23]. Pseudohermaphrodites who have a genetic mutation blocking the production of 5-alpha reductase type II are immune to baldness[19][20][32]. This is the enzyme that converts testosterone into the more potent metabolite dihydrotestosterone (DHT). It was the observation of no baldness in these pseudohermaphrodites which prompted the development of Propecia (finasteride) to treat baldness. The drug binds to and blocks the action of the enzyme 5ar-II, which is produced by the gene SRD5A2. Genetic studies have also identified this gene as causal in the development of AGA. When controlling for age, ethnicity, etc., men with variants of this gene that increase production of the enzyme have a significantly higher risk of going bald[9].

The effects of DHT on the hair follicle are mediated by binding to its receptors, the androgen receptor, this allows the androgen receptor to translocate into the nucleus of the cell where it can bind DNA and regulate gene transcription. The AR, the gene that produces the androgen receptor, shows an even stronger genetic association with baldness than SRD5A2. Polymorphisms of this gene show the strongest association with baldness of any gene. There is a disease called Kennedy disease, which is caused by extended CAG repeats in the AR gene. Repeats reduce the sensitivity of the AR gene to activation. Men with this disease are protected against baldness. The more repeats they have the less likely they are to go bald.[1][9]The application of androgens to hair follicles ex vivo retards their growth.[25][26][27] Even when hair follicle cells are removed and exposed to androgens in vitro it reduces their proliferation, the effect of which is reversed by coculture with an androgen receptor antagonist. Only dermal papilla cells from human and macaque hair follicles which are subject to AGA show reduced hair cell proliferation in response to androgens. It does not affect hair follicles on the back of the head.[10][24] Removing the AR or DHT prevents the gene transcription changes that take place in frontal hair follicles.[2] Treatment with androgens inhibits differentiation of hair follicle stem cells by inhibiting the Wnt pathway.[28]

Bald scalp has higher levels of DHT, AR and SRD5A2 than healthy scalp.[3][4][15] In all primates, men do not go bald before reaching sexual maturity. Macaques go bald within months of reaching puberty when androgens are produced. Their baldness represents a hypoplastic change in the type of hair follicle from terminal to vellus similar ,but in the opposite direction, to the hypoplastic change androgens cause in body hair after puberty. [6][29]. This is due to the known differential growth responses that androgens have on genetically identical hair follicles, which varies due to site-specific epigenetic programming.[30] Men who were castrated as juveniles do not go bald, but when injected with testosterone they do. Cessation of testosterone treatment in eunuchs, or castration of balding men, prevents further baldness, but does not reverse baldness[5]. Finasteride prevents baldness in monkeys.[14] Finasteride and dutasteride are highly selective drugs that inhibit only the enzyme responsible for producing DHT. Finasteride, which reduces scalp DHT by 64%[31], prevents baldness in 86% of men after a 10 year follow up[11], and 99% of Japanese men[12]. The more potent dutasteride halted baldness in 94% of men after 5 year follow up[12]. Genetic knockout of SRD5A2 or AR would prevent it in all men who don’t have a rare mutation in one of the genes downstream of the AR.

1 https://academic.oup.com/bjd/article-abstract/157/2/290/66408662 https://www.nature.com/articles/s41597-022-01846-w3 https://academic.oup.com/jcem/article-abstract/39/6/1012/26855274 https://www.nature.com/articles/s41598-023-48942-45 https://onlinelibrary.wiley.com/doi/10.1002/aja.10007103066 https://link.springer.com/chapter/10.1007/978-3-642-74612-3_187 https://link.springer.com/chapter/10.1007/978-3-642-74612-3_188 https://pubmed.ncbi.nlm.nih.gov/16127116/9 https://www.nature.com/articles/s41467-017-01490-810 https://pubmed.ncbi.nlm.nih.gov/8977424/11 https://pubmed.ncbi.nlm.nih.gov/21910805/12 https://pubmed.ncbi.nlm.nih.gov/38321615/13 https://www.oatext.com/Long-term-(1...3-Japanese-men-with-androgenetic-alopecia.php14 https://pubmed.ncbi.nlm.nih.gov/1309834/15 https://academic.oup.com/jcem/article-abstract/38/5/811/26854011 6 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441445/17 https://link.springer.com/article/10.1007/s00439-006-0317-81 8 https://www.belgraviacentre.com/blog/native-americans-and-hair-loss19 https://pubmed.ncbi.nlm.nih.gov/25321150/ 20 https://www.science.org/doi/10.1126/science.186.4170.121321 https://www.ncbi.nlm.nih.gov/books/NBK430924/ 22 https://karger.com/sad/article/7/2/135/291539/Androgenetic-Alopecia-in-a-Patient-with 23 https://pubmed.ncbi.nlm.nih.gov/8092978/24 https://www.spandidos-publications.com/10.3892/mmr.2015.3478?text=fulltext 25 https://pubmed.ncbi.nlm.nih.gov/2078048/26https://www.eeose.com/UserFiles/Image/files/pdfler/caffeineno_b.pdf 27 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC698966028 https://pubmed.ncbi.nlm.nih.gov/22283397/29 https://pubmed.ncbi.nlm.nih.gov/7035577/ 30 https://pubmed.ncbi.nlm.nih.gov/29046359/31https://www.sciencedirect.com/science/article/pii/S0022202X1552935732https://pubmed.ncbi.nlm.nih.gov/4432067/ (bewerkt)

5-alpha reductase (5AR) inhibitors have barely or no side effects
5ar inhibitors have no side effects
I sended many good studies including meta analyses (The highest level of scientific proof) supporting this claim in this excellent thread

The FDA even did a investigation and found out that 5AR inhibitors have no sexual or depressive side effects

Don’t be scared of the DHT lovers in this forum and their pseudoscientific theories (which lack solid scientific evidence)
Their theories simply don’t happen in reality—it’s just yapping. They simply don’t happen.


WHAT DR NICKGA!! DHT IS NEEDED FOR BONEMASS AND AND..... (yapping)
It already got debunked in this thread (which they stole some of my arguments hehehehehehe) and this debate i had with a disgusting dht lover


NO NOOO NOOOOO BALDING IS CAUSED BY PROLACTIN AND UHH FAPPING!!
We males experience androgenetic alopecia
Balding in males is 99% caused by DHT, ANDROGENS
BALDING IS CAUSED BY HIGH LEVEL OF DHT IN THE SCALP COMBINED WITH HIGH LEVEL OF ANDROGEN RECEPTOR IN THE SCALP

the scalp tension bloodflow theory, the estrogen theory (low estrogen = balding) , the faping theoryy (......) and more
It’s all utter nonsense by the dht lovers
View attachment 3391607
View attachment 3391610View attachment 3391614View attachment 3391620View attachment 3391622View attachment 3391608
THESE PEOPLE ARE IDIOTS , VERY VERY DUMB IN THE PICTURES, IMAGINES ABOVE
including @ConfusedBolivian and @Jonas2k7 who also blamed serum prolactin causing androgenetic alopecia??????

this picturess , imagines are 0.00001 of the Psuedoscience and stupidity in .org


@piec @halloweed @Hexmask @DR. NICKGA
@piec @halloweed @Hexmask @DR. NICKGA
Yo dr Nickga, do you have any tips on regrowing hair? Been on minox already for 2.5 years then switched to fin+oral minox and my hair is way thicker, but areas that were already affected don’t seem to be regrowing.
 
  • +1
Reactions: averagenormie
Buddy boyos, just use finasteride, I'm 18 , started balding last year due to high dht
Genes. I reached norwood 3 almost peaking norwood 4 started taking 5mg minoxidil and 1 mg finasteride daily, all the fear mongering is retarded, the side effects are zero to none,it's been 1 year and my hairline is better than ever. Jfl if you are fellow curry , it is very cheap in india only 1rupee per tablet. cheat code thank me later
 
Last edited:
  • +1
Reactions: DR. NICKGA
If fapping was a cause of MPB, I wouldn't have this hair at my age (31)
 

Attachments

  • 20240328_022415.jpg
    20240328_022415.jpg
    16.2 KB · Views: 25
Buddy boyos, just use finasteride, I'm 18 , started balding last year due to high dht
Genes. I reached norwood 3 almost peaking norwood 4 started taking 5mg minoxidil and 1 mg finasteride daily, all the fear mongering is retarded, the side effects are zero to none,it's been 1 year and my hairline is better than ever. Jfl if you are fellow curry , it is very cheap in india only 1rupee per tablet. cheat code thank me later
The side effects are real
 
only if dht is higher than igf1
 
Yo dr Nickga, do you have any tips on regrowing hair? Been on minox already for 2.5 years then switched to fin+oral minox and my hair is way thicker, but areas that were already affected don’t seem to be regrowing.
0.5 mg dutasteride or wait for more future treatments
 
Wdym almost everyone on dutasteride have a limp dick or on trt
any scientific studies to backup this claim? No?? Alright fuck the out there then

I orgasm everyday while on 0.5 mg dut
 
Sure buddy
Me dick is massive , very very big

Every year its growing massively , more and more gains every year. Its growing rapidly every year . I look at me dick and think "ohh please its huge pleaseee its too thick and big and veiny! Its too big pleasee when do it stop.."

Pleasee godd why is me dick so huge and thick
 
any scientific studies to backup this claim?
 
I have impotence
I told you dude dht maintains your penis together with testosterone, the effect of using 5ar inhibitor and its effect on predisposed men are not known some may do well with test but some need dht also taking it forever doesn't look like a cure
 
Are you fucking retarded?
Please read you own studies , please do that

All me own studies destroyed the fact that 5ar inhibitors cause "sexual side effects"
I sended Even big meta anylysis

This is not even worth a discussion
 
Last edited:
I told you dude dht maintains your penis together with testosterone, the effect of using 5ar inhibitor and its effect on predisposed men are not known some may do well with test but some need dht also taking it forever doesn't look like a cure
Yes finasteride is the cure of 95% of people for 10 years (even more but there is no studies doing more then 10 years)

I told you dude dht maintains your penis together with testosterone, the effect of using 5ar inhibitor and its effect on predisposed men are not known
The effects are very known, barely any side effects
 
the fact that 5ar inhibitors cause "sexual side effects"

This is not even worth a discussion
Don't forget to take cialis and an aromatase inhibitor just to Sexually function well and nut like 5 times at time with only test
 
Yes finasteride is the cure of 95% of people for 10 years (even more but there is no studies doing more then 10 years)


The effects are very known, barely any side effects
What about dut? How can you free the system from the drug quickly so you can take fin instead as its faster to clean up and you can stop it anytime?
 
Don't forget to take cialis and an aromatase inhibitor just to Sexually function well and nut like 5 times at time with only test
Conclusions

Finasteride and dutasteride are approved for use in the treatment of men with symptomatic BPH and androgenic alopecia and are also under study in ongoing prostate cancer prevention trials. It was shown that treatment with 5ARIs results in a reduction in median serum DHT levels by 60%–93% after 2 years (Imperato-McGinley et al, 1974; Uygur et al, 1998; Andriole and Kirby, 2003; Clark et al, 2004; Marberger et al, 2006). According to 13 randomized studies in which finasteride was used alone, erectile problems occurred in 3% of the men studied long term (AUA Practice Guidelines Committee, 2003). This percentage of ED would seem minimal, and it is also noteworthy that this adverse event diminished by half over time in men taking finasteride (Stoner, 1994; Roehrborn et al, 2004; Moinpour et al, 2007)

please read you own studies

What about dut? How can you free the system from the drug quickly so you can take fin instead as its faster to clean up and you can stop it anytime?
That is a another case, but since you are very high inhib, a pussy i think you should take neither of both

Just take nothing at all, pussy
 
1.However, a substantial body of evidence exists which points to serious and potentially ill-health effects of 5α-RIs' therapy. These include loss or reduced libido, erectile dysfunction, orgasmic and ejaculatory dysfunction (Table 2) [99], development of high grade PCa tumors (Fig. 4), potential negative cardiovascular events, and depression. The side effects are potentially harmful in some individuals and in young men may be persistent or irreversible [100].
2.Lugg et al (1995) further investigated which androgen is vital for function of the penis with respect to erectile function. They performed a study to determine whether the T effects on erectile function are mediated via its conversion to DHT. In their study, castrated rats were implanted with silastic brand silicon tubing containing T or DHT with or without daily injections of the 5ARI finasteride. Orchiectomy reduced the electrical field stimulation-induced erectile response by 50% in comparison with intact rats, and T restored this decrease to normal. When finasteride was given to these T-treated castrated rats, erectile response was not restored. DHT was as effective as T in restoring response to stimulation in castrates, and this effect was not decreased by finasteride (Lugg et al, 1995). The results seem to corroborate the information of Bradshaw and associates (1981). The data suggested that DHT is the active androgen that prevents erectile failure in castrated rats.
3.For this purpose, rats were separated into 5 groups: sham, castrated alone, and castrated receiving T, DHT, or T with the 5ARI finasteride. Both T and DHT effectively restored the erectile response to normal. NOS activity and the amount of neuronal NOS (nNOS) mRNA were also reduced in castrated rats but restored by both T and DHT replacement. Although there was no significant difference in NOS activity between the androgens, nNOS mRNA expression was higher in rats treated with DHT. Strikingly, there were no effects of T in rats treated with finasteride, since the ratio of maximum intracavernosal pressure to systolic blood pressure (ICPmax/SBP ratio), NOS activity, and amount of nNOS mRNA were decreased (Park et al, 1999).
3.Finasteride may be safer to treat alopecia but not dut:
When the results of clinical studies are examined, it is not clearly evident that 5ARIs have a negative effect in men as seen in animal studies. This may be explained by the fact that in animals DHT levels were either zero or normal. It was shown that treatment with 5ARIs results in a reduction in median serum DHT levels in men by 60%–93% after 2 years (Imperato-McGinley et al, 1974; Uygur et al, 1998; Andriole and Kirby, 2003; Clark et al, 2004; Marberger et al, 2006). The 5ARIs cause a reduction in DHT levels but do not eliminate it completely from the circulation. For example, since finasteride inhibits only type II 5 α-reductase receptors, circulating DHT is only reduced by two-thirds (Thigpen et al, 1993a; Thigpen et al, 1993b; Gisleskog et al, 1998)
 

Attachments

  • Screenshot_2025-01-20-23-14-26-754_com.android.chrome-edit.jpg
    Screenshot_2025-01-20-23-14-26-754_com.android.chrome-edit.jpg
    288 KB · Views: 15
Conclusions

Finasteride and dutasteride are approved for use in the treatment of men with symptomatic BPH and androgenic alopecia and are also under study in ongoing prostate cancer prevention trials. It was shown that treatment with 5ARIs results in a reduction in median serum DHT levels by 60%–93% after 2 years (Imperato-McGinley et al, 1974; Uygur et al, 1998; Andriole and Kirby, 2003; Clark et al, 2004; Marberger et al, 2006). According to 13 randomized studies in which finasteride was used alone, erectile problems occurred in 3% of the men studied long term (AUA Practice Guidelines Committee, 2003). This percentage of ED would seem minimal, and it is also noteworthy that this adverse event diminished by half over time in men taking finasteride (Stoner, 1994; Roehrborn et al, 2004; Moinpour et al, 2007)

please read you own studies


That is a another case, but since you are very high inhib, a pussy i think you should take neither of both

Just take nothing at all, pussy
Are you fucking stupid nigga? I'm saying that it depends on the person high T mf with very little to no dht may be affected but some one with normal levels and lower dht or average might do very well, I'm on dut for almost a year and I experienced the nasty side effects
 

Similar threads

EGGY 1671u32g
Replies
12
Views
322
Mike141
Mike141
larox.psl
Replies
28
Views
822
mattmogstomumbai
mattmogstomumbai
fluoride1337
Replies
12
Views
343
KILLALLJEWS
KILLALLJEWS
A
Replies
5
Views
107
moreplatesmoreweigh
moreplatesmoreweigh
appeal
Replies
173
Views
3K
DR. NICKGA
DR. NICKGA

Users who are viewing this thread

Back
Top